Search results for "Polymorphism"

showing 10 items of 1968 documents

Genome-wide Association Studies Identify Genetic Loci Associated with Albuminuria in Diabetes

2016

Elevated concentrations of albumin in the urine, albuminuria, are a hallmark of diabetic kidney disease and are associated with an increased risk for end-stage renal disease and cardiovascular events. To gain insight into the pathophysiological mechanisms underlying albuminuria, we conducted meta-analyses of genome-wide association studies and independent replication in up to 5,825 individuals of European ancestry with diabetes and up to 46,061 without diabetes, followed by functional studies. Known associations of variants in CUBN, encoding cubilin, with the urinary albumin-to-creatinine ratio (UACR) were confirmed in the overall sample (P = 2.4 × 10−10). Gene-by-diabetes interactions were…

Male0301 basic medicinediabetes geneEndocrinology Diabetes and MetabolismGenome-wide association studyKidneyGLOMERULAR-FILTRATION-RATECathepsin CGene Knockout TechniquescubilinSettore MED/14 - NEFROLOGIADiabetic NephropathiesMODULATES PROTEINURIAddc:616HERITABILITYDiabetesGenetics/Genomes/Proteomics/MetabolomicsMiddle AgedRISK POPULATION COHORTS3. Good healthINSIGHTSKidney TubulesFemaleSulfotransferasesmedicine.symptomRAB38AdultEXPRESSIONmedicine.medical_specialtyRenal functionReceptors Cell Surface610 Medicine & healthSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotidealbuminuriaDiabetes Mellitus Experimental03 medical and health sciencesDiabetes mellitusInternal medicineInternal MedicinemedicineAnimalsHumansGenetic Predisposition to DiseaseAgedMORTALITYKIDNEY-DISEASEmedicine.diseaseCubilinRatsMinor allele frequency030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2rab GTP-Binding ProteinsCOLLABORATIVE METAANALYSISAlbuminuria570 Life sciences; biologyalbuminuria diabetes cubilinGenome-Wide Association StudyKidney disease
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CNTN6 mutations are risk factors for abnormal auditory sensory perception in autism spectrum disorders

2017

International audience; Contactin genes CNTN5 and CNTN6 code for neuronal cell adhesion molecules that promote neurite outgrowth in sensory-motor neuronal pathways. Mutations of CNTN5 and CNTN6 have previously been reported in individuals with autism spectrum disorders (ASDs), but very little is known on their prevalence and clinical impact. In this study, we identified CNTN5 and CNTN6 deleterious variants in individuals with ASD. Among the carriers, a girl with ASD and attention-deficit/hyperactivity disorder was carrying five copies of CNTN5. For CNTN6, both deletions (6/1534 ASD vs 1/8936 controls; P=0.00006) and private coding sequence variants (18/501 ASD vs 535/33480 controls; P=0.000…

Male0301 basic medicinegenetic structuresAutism Spectrum Disorder[ SDV.MHEP.PSM ] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.MHEP.PSM] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental healthmedicine.disease_causeChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGeneticsMutationPsychiatry and Mental healthSchizophrenia[ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology[ SCCO.NEUR ] Cognitive science/NeuroscienceAuditory PerceptionMedical geneticsOriginal ArticleFemalePsychopharmacologymedicine.symptomPsychologyAdultmedicine.medical_specialtyAdolescentDNA Copy Number Variations[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsPolymorphism Single Nucleotidebehavioral disciplines and activities03 medical and health sciencesCellular and Molecular NeuroscienceContactinsmental disordersmedicineHumansDementiaGenetic Predisposition to DiseaseMolecular Biology[SCCO.NEUR]Cognitive science/Neuroscience[SCCO.NEUR] Cognitive science/NeuroscienceHyperacusis[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[ SDV.SP.PHARMA ] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologymedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAttention Deficit Disorder with Hyperactivity[SDV.MHEP.PSM]Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental healthMutationBehavioral medicine[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyAutismNeuroscienceMolecular Psychiatry
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MAOA-VNTR polymorphism modulates context-dependent dopamine release and aggressive behavior in males

2016

A recent [F-18]FDOPA-PET study reports negative correlations between dopamine synthesis rates and aggressive behavior. Since dopamine is among the substrates for monoamine oxidase A (MAOA), this investigation examines whether functional allelic variants of the MAOA tandem repeat (VNTR) promotor polymorphism, which is known to modulate aggressive behavior, influences dopamine release and aggression in response to violent visual stimuli. We selected from a genetic prescreening sample, strictly case-matched groups of 2 x 12 healthy male subjects with VNTRs predictive of high (MAOA-High) and low (MAOA-Low) MAOA expression. Subjects underwent pairs of PET sessions (dopamine D-2/3 ligand [F-18]DM…

Male0301 basic medicinemedicine.medical_specialtyGenotypeCognitive NeuroscienceDopamineContext (language use)Polymorphism Single NucleotideDevelopmental psychologyYoung Adult03 medical and health sciences0302 clinical medicineDopaminePolymorphism (computer science)Dopamine receptor D2Internal medicineImage Processing Computer-AssistedmedicineHumansMAOAYoung adultMonoamine OxidasebiologyAggressionDopaminergicBrainDMFPAggression030104 developmental biologyEndocrinologyPETNeurologyPositron-Emission Tomographybiology.proteinmedicine.symptomMonoamine oxidase APsychology030217 neurology & neurosurgerymedicine.drug
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Polymorphisms of Pro-Inflammatory IL-6 and IL-1β Cytokines in Ascending Aortic Aneurysms as Genetic Modifiers and Predictive and Prognostic Biomarkers

2021

Background: Previous studies have demonstrated that polymorphisms involved in immune genes can affect the risk, pathogenesis, and outcome of thoracic ascending aortic aneurysms (TAAA). Here, we explored the potential associations of five functional promoter polymorphisms in interleukin-6 (IL-6), IL-1B, IL-1A, IL-18, and Tumor necrosis factor (TNF)A genes with TAAA. Methods: 144 TAAA patients and 150 age/gender matched controls were typed using KASPar assays. Effects on telomere length and levels of TAAA related histopathological and serological markers were analyzed. Results: Significant associations with TAAA risk were obtained for IL-6 rs1800795G&gt

Male0301 basic medicinemedicine.medical_specialtyInterleukin-1betamedial cell apoptosisSingle-nucleotide polymorphism030204 cardiovascular system & hematologyrs16944MicrobiologyPolymorphism Single NucleotideBiochemistryGastroenterologyArticleProinflammatory cytokinePathogenesis03 medical and health sciences0302 clinical medicineAneurysmInternal medicineGenotypeelastic fragmentationmedicinetelomere lengthHumansInterleukin 6thoracic ascending aortic aneurysmsMolecular BiologyAgedAortic Aneurysm ThoracicbiologyInterleukin-6business.industryMMP9Prognosismedicine.diseasers1800795QR1-502Settore MED/23030104 developmental biologyproinflammatory cytokinescystic medial changesbiology.proteinCytokinesBiomarker (medicine)FemaleTumor necrosis factor alphaInflammation MediatorsbusinessBiomarkersBiomolecules
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Mean Platelet Volume and Arterial Stiffness - Clinical Relationship and Common Genetic Variability

2017

AbstractVessel wall stiffening is an important clinical parameter, but it is unknown whether platelets, key elements in the pathogenesis of arterial thrombosis, are associated with arterial stiffness. The present studies sought to determine whether mean platelet volume (MPV), a potential marker of platelet activation, is linked to vascular elasticity as assessed by the augmentation index (AIx), in 15,010 individuals from the population-based Gutenberg Health Study. Multivariable analysis showed that MPV in both males (β 0.776; 95thCI [0.250;1.16]; p = 0.0024) and females (β 0.881[0.328;1.43]; p = 0.0018) is strongly associated with AIx. Individuals with MPV and AIx above the sex-specific me…

Male0301 basic medicinemedicine.medical_specialtyPopulationKaplan-Meier Estimate030204 cardiovascular system & hematologyPolymorphism Single NucleotideArticle03 medical and health sciencesSex FactorsVascular Stiffness0302 clinical medicineGUTENBERG HEALTHDEFICIENTINFLAMMATIONRisk FactorsInternal medicinemedicineHumansPlateletPlatelet activationMean platelet volumeeducationMETAANALYSISeducation.field_of_studyMultidisciplinaryHYPERTENSIONbusiness.industryProportional hazards modelHazard ratioGenetic VariationCROSS-SECTIONAL RELATIONSmedicine.diseaseThrombosisElasticityREACTIVITY030104 developmental biologyISCHEMIC-STROKEATHEROSCLEROSISCardiovascular DiseasesArterial stiffnessCardiologyFemalebusinessMean Platelet VolumeVASCULAR FUNCTIONBiomarkers
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Intragenic FMR1 disease-causing variants: a significant mutational mechanism leading to Fragile-X syndrome

2017

International audience; Fragile-X syndrome (FXS) is a frequent genetic form of intellectual disability (ID). The main recurrent mutagenic mechanism causing FXS is the expansion of a CGG repeat sequence in the 5'-UTR of the FMR1 gene, therefore, routinely tested in ID patients. We report here three FMR1 intragenic pathogenic variants not affecting this sequence, identified using high-throughput sequencing (HTS): a previously reported hemizygous deletion encompassing the last exon of FMR1, too small to be detected by array-CGH and inducing decreased expression of a truncated form of FMRP protein, in three brothers with ID (family 1) and two splice variants in boys with sporadic ID: a de novo …

Male0301 basic medicinemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesdiagnosisRNA SplicingBiologymedicine.disease_causePolymorphism Single NucleotideArticleFragile X Mental Retardation Protein03 medical and health sciencesExonGenetic linkageplacebo-controlled trial[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansgeneGenetics (clinical)GeneticsMutationintron 10SiblingsMiddle Agedmedicine.diseaseFMR1Human genetics3. Good healthFragile X syndromedevelopmental delayof-the-literature030104 developmental biologyintellectual disabilityFragile X SyndromeMutationmental-retardationMedical geneticsFemalepoint mutationdouble-blind[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Patients experiencing statin-induced myalgia exhibit a unique program of skeletal muscle gene expression following statin re-challenge

2017

Statins, the 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase inhibitors, are widely prescribed for treatment of hypercholesterolemia. Although statins are generally well tolerated, up to ten percent of statin-treated patients experience myalgia symptoms, defined as muscle pain without elevated creatinine phosphokinase (CPK) levels. Myalgia is the most frequent reason for discontinuation of statin therapy. The mechanisms underlying statin myalgia are not clearly understood. To elucidate changes in gene expression associated with statin myalgia, we compared profiles of gene expression in skeletal muscle biopsies from patients with statin myalgia who were undergoing statin re-challenge (cases)…

Male0301 basic medicinemyalgiaGene Expressionlcsh:MedicineApoptosis030204 cardiovascular system & hematologyPathology and Laboratory MedicineBioinformaticsBiochemistry0302 clinical medicineMedicine and Health SciencesGene Regulatory Networkslcsh:ScienceMusculoskeletal SystemEnergy-Producing OrganellesMyositisRegulation of gene expressionMultidisciplinaryCell DeathbiologyMusclesDrugsMiddle AgedMitochondriaCell ProcessesHMG-CoA reductaseFemalelipids (amino acids peptides and proteins)AnatomyCellular Structures and Organellesmedicine.symptomResearch ArticleSenescencemedicine.medical_specialtyStatinmedicine.drug_classPainBioenergeticsPolymorphism Single Nucleotide03 medical and health sciencesSigns and SymptomsDiagnostic MedicineInternal medicineGeneticsmedicineHumansGene Regulationcardiovascular diseasesMuscle SkeletalAgedPharmacologybusiness.industrylcsh:RStatinsBiology and Life SciencesComputational Biologynutritional and metabolic diseasesMyalgiaCell Biologymedicine.disease030104 developmental biologyEndocrinologyGene Expression RegulationSkeletal MusclesLeukocytes Mononuclearbiology.proteinProtein prenylationlcsh:QHydroxymethylglutaryl-CoA Reductase InhibitorsSLCO1B1businessPLOS ONE
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NS5A gene analysis by next generation sequencing in HCV nosocomial transmission clusters of HCV genotype 1b infected patients

2019

Background: The aim of the study was to investigate the intra-host variability through next-generation-sequencing (NGS) of the NS5A-gene in nosocomial transmission-clusters observed in two Italian hospitals among hepatitis C virus (HCV)-genotype-1b infected patients. Methods: HCV-sequencing was performed by Sanger-sequencing (NS3 + NS5A + NS5B) and by NGS (NS5A, MiSeq-Illumina) in 15 HCV-1b infected patients [five acute with onco-hematologic-disease and 10 (4/6 acute/chronic) with &beta

Male0301 basic medicinevirusesDrug ResistanceHepacivirusViral Nonstructural Proteinsmedicine.disease_causeSettore MED/42 - Igiene Generale E ApplicataGastroenterologySettore MED/07chemistry.chemical_compound0302 clinical medicineGenotype 1bMedicineVirallcsh:QH301-705.5PhylogenyCross Infectionnosocomial transmissionGastroenterologyHigh-Throughput Nucleotide Sequencingvirus diseasesHCV; NGS; acute infection; chronic infection; nosocomial transmission; sequencing; Acute Disease; Adult; Amino Acid Substitution; Antiviral Agents; Blood Transfusion; Chronic Disease; Cross Infection; Drug Resistance Viral; Female; Genotype; Hepacivirus; Hepatitis C; High-Throughput Nucleotide Sequencing; Host-Pathogen Interactions; Humans; Interferons; Male; Middle Aged; Phylogeny; Polymorphism Single Nucleotide; Viral Nonstructural Proteins; beta-ThalassemiaSingle NucleotideGeneral MedicinesequencingMiddle AgedHepatitis CNGSAcute DiseaseHost-Pathogen InteractionsHCVFemale030211 gastroenterology & hepatologyAdultmedicine.medical_specialtyGenotypeHepatitis C virusViral quasispeciesPolymorphism Single NucleotideAntiviral AgentsArticleDNA sequencing03 medical and health sciencesInternal medicineDrug Resistance ViralHumansBlood TransfusionPolymorphismNS5ANS5BGeneHepatologybusiness.industryNosocomial transmissionbeta-Thalassemiabiochemical phenomena metabolism and nutritionchronic infectionVirologydigestive system diseasesChronic infection030104 developmental biologyAmino Acid Substitutionchemistrylcsh:Biology (General)Chronic DiseaseHCV; NGS; acute infection; chronic infection; nosocomial transmission; sequencingInterferonsbusinessacute infectionDigestive and Liver Disease
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Genetic prediction of ICU hospitalization and mortality in COVID‐19 patients using artificial neural networks

2021

There is an unmet need of models for early prediction of morbidity and mortality of Coronavirus disease-19 (COVID-19). We aimed to a) identify complement-related genetic variants associated with the clinical outcomes of ICU hospitalization and death, b) develop an artificial neural network (ANN) predicting these outcomes and c) validate whether complement-related variants are associated with an impaired complement phenotype. We prospectively recruited consecutive adult patients of Caucasian origin, hospitalized due to COVID-19. Through targeted next-generation sequencing, we identified variants in complement factor H/CFH, CFB, CFH-related, CFD, CD55, C3, C5, CFI, CD46, thrombomodulin/THBD, …

Male0304 Medicinal and Biomolecular Chemistry 0601 Biochemistry and Cell Biology 1103 Clinical SciencesBiochemistry & Molecular BiologyGreeceModels GeneticThrombomodulinCOVID-19Complement System ProteinsCell BiologyMiddle AgedPolymorphism Single NucleotideHospitalizationSettore ICAR/09 - Tecnica Delle CostruzioniIntensive Care UnitsComplement Factor HHumansMolecular MedicineFemaleNeural Networks ComputerMorbidityartificial intelligence complement complement inhibition COVID-19 genetic susceptibility SARS-CoV2Complement ActivationJournal of Cellular and Molecular Medicine
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Association between the polymorphisms of TLR4 and CD14 genes and Alzheimer's disease.

2008

Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease which in Western society mainly accounts for clinical dementia. Inflammation plays a key role in AD and dissecting the genetics of inflammation may provide an answer to the possible treatment. Hence, the better understanding of different molecular and cellular inflammatory mechanisms is crucial for complete knowledge of AD pathophysiology, and for its prevention and drug therapy. Accordingly, in the present study we evaluated whether the pro-inflammatory polymorphisms of lipopolysaccaride-receptors, +896A/G Toll-Like Receptor (TLR4) and -260C/T CD14, are risk factors for AD. The study included both 626 AD …

MaleALZHEIMER'S DISEASEINFLAMMATIONINNATE IMMUNITYTLR4CD14Lipopolysaccharide ReceptorsInflammationSingle-nucleotide polymorphismDiseaseSystemic inflammationPolymorphism Single NucleotideSeverity of Illness IndexDegenerative diseaseINFLAMMATIONAlzheimer DiseaseRisk FactorsDrug DiscoverymedicineDementiaSNPHumansTLR4AgedPharmacologyAged 80 and overbusiness.industryMiddle Agedmedicine.diseaseToll-Like Receptor 4ItalyALZHEIMER'S DISEASEImmunologyINNATE IMMUNITYFemalemedicine.symptomAlzheimer's diseasebusinessCD14
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